Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
Department of Psychology and Neuroscience, Baylor University, Waco, Texas.
Psychophysiology. 2018 Dec;55(12):e13265. doi: 10.1111/psyp.13265. Epub 2018 Jul 30.
Recent evidence indicates that cerebral autoregulation (CA) might be more pressure passive than previously thought. That is, cerebral blood flow, traditionally thought to be regulated independently of prevailing mean arterial pressure (MAP), might fluctuate, to some extent, as a function of MAP. However, due to limitations associated with experimental usage of pharmaceuticals to manipulate MAP and inconsistent control of arterial carbon dioxide, questions remain regarding the MAP-cerebral blood flow relationship, especially during typical daily activities that alter MAP. Therefore, the current study aimed to assess CA using a nonpharmacological acute psychological stress task to augment MAP, while at the same time controlling for end-tidal carbon dioxide (P CO ). Twenty-five healthy young adults completed a stressful task while continuous measures of MAP, middle cerebral artery blood flow velocity (MCAv), and P CO were recorded. Slope values obtained from hierarchical linear regression were used to assess the strength of the MAP-MCAv relationship and control for P CO . The stress task significantly increased MAP (p < 0.001) and MCAv (p < 0.001), and decreased P CO (p = 0.05). For every 10 mmHg task-induced increase in MAP, MCAv increased by ≈3.5%; task-induced changes in P CO did not appreciably change the MAP-MCAv relationship. Greater task-induced MAP responses were significantly related to decreased MAP-MCAv slope values, consistent with CA. These data support the hypothesis that CA is more pressure passive than previously thought and provide initial evidence indicating that a pressure-passive MAP-MCAv relationship may play a role in the observed associations between MAP stress responses, stroke, and cerebrovascular disease.
最近的证据表明，脑自动调节（CA）可能比以前认为的更具压力被动性。也就是说，传统上认为不受当前平均动脉压（MAP）调节的脑血流，可能会在一定程度上随着 MAP 的波动而波动。然而，由于在实验中使用药物来操纵 MAP 和动脉二氧化碳（P CO ）的控制不一致，导致关于 MAP-脑血流关系的问题仍然存在，尤其是在改变 MAP 的典型日常活动中。因此，本研究旨在使用非药理学急性心理应激任务来增加 MAP 来评估 CA，同时控制呼气末二氧化碳（P CO ）。25 名健康年轻成年人在完成一项有压力的任务的同时，连续记录 MAP、大脑中动脉血流速度（MCAv）和 P CO 的测量值。使用分层线性回归获得的斜率值来评估 MAP-MCAv 关系的强度，并控制 P CO 。应激任务显著增加了 MAP（p<0.001）和 MCAv（p<0.001），并降低了 P CO （p=0.05）。MAP 每增加 10mmHg，MCAv 增加约 3.5%；P CO 的任务诱导变化并没有明显改变 MAP-MCAv 关系。更大的任务诱导 MAP 反应与降低的 MAP-MCAv 斜率值显著相关，这与 CA 一致。这些数据支持 CA 比以前认为的更具压力被动性的假设，并提供了初步证据表明，压力被动性的 MAP-MCAv 关系可能在观察到的 MAP 应激反应、中风和脑血管疾病之间的关联中发挥作用。
